1,721,180 research outputs found

    Economic conditions predict prevalence of West Nile virus.

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    Understanding the conditions underlying the proliferation of infectious diseases is crucial for mitigating future outbreaks. Since its arrival in North America in 1999, West Nile virus (WNV) has led to population-wide declines of bird species, morbidity and mortality of humans, and expenditures of millions of dollars on treatment and control. To understand the environmental conditions that best explain and predict WNV prevalence, we employed recently developed spatial modeling techniques in a recognized WNV hotspot, Orange County, California. Our models explained 85-95% of the variation of WNV prevalence in mosquito vectors, and WNV presence in secondary human hosts. Prevalence in both vectors and humans was best explained by economic variables, specifically per capita income, and by anthropogenic characteristics of the environment, particularly human population and neglected swimming pool density. While previous studies have shown associations between anthropogenic change and pathogen presence, results show that poorer economic conditions may act as a direct surrogate for environmental characteristics related to WNV prevalence. Low-income areas may be associated with higher prevalence for a number of reasons, including variations in property upkeep, microhabitat conditions conducive to viral amplification in both vectors and hosts, host community composition, and human behavioral responses related to differences in education or political participation. Results emphasize the importance and utility of including economic variables in mapping spatial risk assessments of disease

    Pathogen-mediated evolution of immunogenetic variation in plains zebra (Equus quagga) of southern Africa

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    In this thesis, I examined the evolution of two equine Major Histocompatibility Complex (MHC) genes, DRA and DQA, over the history of the genus Equus and across free-ranging plains zebra (E. quagga) populations of southern Africa: Etosha National Park (ENP), Namibia and Kruger National Park (KNP), South Africa. Furthermore, I evaluated the relationships between the DRA locus and parasite intensity in E. quagga of ENP, to elucidate the mechanisms by which parasites have shaped diversity at the MHC. In equids, the full extent of diversity and selection on the MHC in wild populations is unknown. Therefore, in this study, I molecularly characterized MHC diversity and selection across equid species to shed light on its mode of evolution in Equus and to identify specific sites under positive selection. Both the DRA and DQA exhibited a high degree of polymorphism and more intriguingly, greater allelic diversity was observed at the DRA than has previously been shown in any other vertebrate taxon. Global selection analyses of both loci indicated that the majority of codon sites are under purifying selection which may be explained by functional constraints on the protein. However, maximum likelihood based codon models of selection, allowing for heterogeneity in selection across codons, suggested that selective pressures varied across sites. Furthermore, at the DQA locus, all sites predicted to be under positive selection were antigen binding sites, implying that a few selected amino acid residues may play a significant role in equid immune function. Observations of trans-species polymorphisms and elevated genetic diversity were concordant with the hypothesis that balancing selection is acting on these genes. Over the past half century, the role of neutral versus selective processes in shaping genetic diversity has been at the center of an ongoing dialogue among evolutionary biologists. To determine the relative influence of demography versus selection on the DRA and DQA loci, I contrasted diversity patterns of neutral and MHC data across the E. quagga populations of ENP and KNP. Neutrality tests, along with observations of elevated diversity and low differentiation across populations relative to nuclear intron data, provided further evidence for balancing selection at these loci among E. quagga populations. However, at the DRA locus, differentiation was comparable to results at microsatellite loci. Furthermore, zebra in ENP exhibited reduced levels of diversity relative to KNP due to a highly skewed allele frequency distribution that could not be explained by demography. These findings were indicative of spatially heterogeneous selection and suggested directional selection and local adaptation at the DRA locus. There still remains a great deal of discussion over the mechanisms by which pathogens preserve immune gene diversity. The leading hypotheses that have been predominantly considered are: (i) heterozygote advantage (i.e. overdominant selection), (ii) rare allele advantage (i.e. frequency-dependent selection), and (iii) spatiotemporally fluctuating selection. An increasing number of studies have investigated MHC-parasite relationships to reconcile this debate, with conflicting results. To elucidate the mechanism driving the population-level patterns of diversity at the DRA locus, I examined relationships between this locus and both gastrointestinal (GI) and ectoparasite intensity in plains zebra of ENP. I discovered antagonistic pleiotropic effects of particular DRA alleles, with rare alleles predicting increased GI parasitism and common alleles associated with higher tick burdens. These results supported a frequency-dependent process and because maladaptive 'susceptibility alleles' were found at reduced frequencies, suggested that GI parasites exert strong selective pressure at this locus. Furthermore, heterozygote advantage also played a role in decreasing GI parasite burden, but only when a common allele was paired with a more divergent allele, implying that frequency-dependent and overdominant selection are acting in synchrony. These results indicated that an immunogenetic tradeoff may modulate resistance/susceptibility to parasites in this system, such that with MHC-based resistance to GI parasitism, a fitness cost is incurred to the host in the form of increased ectoparasite susceptibility. It is also suggested that these selective mechanisms are not mutually exclusive. (Abstract shortened by UMI.

    Contact with domestic dogs increases pathogen exposure in endangered African wild dogs (Lycaon pictus).

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    BACKGROUND:Infectious diseases have contributed to the decline and local extinction of several wildlife species, including African wild dogs (Lycaon pictus). Mitigating such disease threats is challenging, partly because uncertainty about disease dynamics makes it difficult to identify the best management approaches. Serious impacts on susceptible populations most frequently occur when generalist pathogens are maintained within populations of abundant (often domestic) "reservoir" hosts, and spill over into less abundant host species. If this is the case, disease control directed at the reservoir host might be most appropriate. However, pathogen transmission within threatened host populations may also be important, and may not be controllable by managing another host species. METHODOLOGY/PRINCIPAL FINDINGS:We investigated interspecific and intraspecific transmission routes, by comparing African wild dogs' exposure to six canine pathogens with behavioural measures of their opportunities for contact with domestic dogs and with other wild dogs. Domestic dog contact was associated with exposure to canine parvovirus, Ehrlichia canis, Neospora caninum and perhaps rabies virus, but not with exposure to canine distemper virus or canine coronavirus. Contact with other wild dogs appeared not to increase the risk of exposure to any of the pathogens. CONCLUSIONS/SIGNIFICANCE:These findings, combined with other data, suggest that management directed at domestic dogs might help to protect wild dog populations from rabies virus, but not from canine distemper virus. However, further analyses are needed to determine the management approaches--including no intervention--which are most appropriate for each pathogen

    Anticoagulant rodenticides on our public and community lands: spatial distribution of exposure and poisoning of a rare forest carnivore.

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    Anticoagulant rodenticide (AR) poisoning has emerged as a significant concern for conservation and management of non-target wildlife. The purpose for these toxicants is to suppress pest populations in agricultural or urban settings. The potential of direct and indirect exposures and illicit use of ARs on public and community forest lands have recently raised concern for fishers (Martes pennanti), a candidate for listing under the federal Endangered Species Act in the Pacific states. In an investigation of threats to fisher population persistence in the two isolated California populations, we investigate the magnitude of this previously undocumented threat to fishers, we tested 58 carcasses for the presence and quantification of ARs, conducted spatial analysis of exposed fishers in an effort to identify potential point sources of AR, and identified fishers that died directly due to AR poisoning. We found 46 of 58 (79%) fishers exposed to an AR with 96% of those individuals having been exposed to one or more second-generation AR compounds. No spatial clustering of AR exposure was detected and the spatial distribution of exposure suggests that AR contamination is widespread within the fisher's range in California, which encompasses mostly public forest and park lands Additionally, we diagnosed four fisher deaths, including a lactating female, that were directly attributed to AR toxicosis and documented the first neonatal or milk transfer of an AR to an altricial fisher kit. These ARs, which some are acutely toxic, pose both a direct mortality or fitness risk to fishers, and a significant indirect risk to these isolated populations. Future research should be directed towards investigating risks to prey populations fishers are dependent on, exposure in other rare forest carnivores, and potential AR point sources such as illegal marijuana cultivation in the range of fishers on California public lands
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